Testicular function and bone in young men with severe childhood-onset obesity.

Background: Previous studies suggest increased risk for hypoandrogenism and fractures in men with obesity. We aimed to describe the effects of severe childhood-onset obesity on the cross talk between metabolic state, testes and skeleton at late puberty. Methods: A cohort of adolescent and young adu...

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Main Authors: Anand-Ivell, Ravinder, Ivell, Richard, Laakso, Saila, Viljakainen, Heli, Lipsanen-Nyman, Marita, Turpeinen, Ursula, Ivaska, Kaisa K, Mäkitie, Outi
Format: Article
Published: Karger 2018
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Online Access:https://eprints.nottingham.ac.uk/51489/
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Summary:Background: Previous studies suggest increased risk for hypoandrogenism and fractures in men with obesity. We aimed to describe the effects of severe childhood-onset obesity on the cross talk between metabolic state, testes and skeleton at late puberty. Methods: A cohort of adolescent and young adult males with severe childhood-onset obesity (n=21, mean age 18.5 yrs) and an age-matched control group were assessed for testicular hormones and DXA-derived bone mass. Results: Current median body mass indexes for the obese and control subjects were 37.4 kg/m2 and 22.9 kg/m2. Severe early-onset obesity manifested with lower free testosterone [median (inter-quartile range) 244 (194–332) vs. 403 (293–463) pmol/l, P=0.002]. Lower insulin-like 3 [1.02 (0.82–1.23) vs. 1.22 (1.01–1.46) ng/mL, P=0.045] and lower ratio of testosterone to LH [2.81 (1.96 – 3.98) vs. 4.10 (3.03 – 5.83) nM/IU, P=0.008] suggested disrupted Leydig cell function. Degree of current obesity correlated inversely with free testosterone (τ=-0.516, P=0.003), which in turn correlated positively with bone area at all measurement sites in males with childhood-onset obesity. Conclusions: Severe childhood-onset obesity associates with impaired Leydig cell function in young men and lower free testosterone may contribute to impaired bone growth.